Mutations are now known in Drosophila that interfere with a wide variety of meiotic chromosomal functions, including the frequency and distribution of exchanges, distributive and exchange segregation, and both reductional and equational disjunction at both the first and second divisions. Moreover, the analyses of such meiotic mutants have elucidated a number of normal cellular phenomena (see, for some specification, the accompanying "Progress Report"). Nevertheless, certain potentially very informative classes of meiotic mutant have, for technical reasons, thus far not been recovered. Foremost among these are single-gene mutations that substantially increase the amount of meiotic recombination. That "recombination-enhancing" meiotic mutants can be induced is attested to by the fortuitous recovery of several unanalyzably weak examples, as well as by interchromosomal effects that can result in dramatic increases in crossing-over. We, therefore, will attempt to isolate and study a collection of EMS-induced, autosomal, recombination-enhancing meiotic mutants. We plan to screen for mutants that increase crossing-over and/or decrease nondisjunction in females that also carry known meiotic mutants -- any of several different recombination- defectives, or disjunction-defectives that cause the nondisjunction of no-exchange tetrads only. A second hitherto unrepresented category of mutant -- the existence of which is conceivable but problematic -- is composed of mutants that eliminate or attenuate mitotic pairing. We will look for "mitotic asynaptics" by screening for suppressors of zeste-white interactions which seem to depend on normal mitotic pairing. In addition to screening for new classes of meiotic mutants, we will continue our ongoing analyses of meiosis and development.